This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. SIV infection in Chinese rhesus macaque (ChRM) results in high frequency of long-term nonprogressing macaques (LTNP). We used this model for continuous study of the role of natural killer (NK) cells in the establishment of long-term nonprogressing state in LTNP ChRM. Recently, to investigate gene expression in NK cells at different status of SIV infection, we used rhesus specific gene array chips for microarray assay. We purified NK cells in peripheral blood from the LTNP and normal progressors (NP) using CD8+, CD16+ beads. CD16 is a low affinity receptor that recognizes IgG as aggregates surrounding multivalent antigens during late immune responses. Remarkably, in comparison with NP, NK cells in LTNP had high up-regulation of CD16 (FcrRIIIa), the gene that was important for the ADCC immune responses. However, the downstream src-family kinase LCK/Fyn was downregulated that may moderate the overall NK cell activation to a relatively low level. Lower NK cell activation may avoid inducing general immune activation, which is possibly the main contributor of low viral status in the LTNP. NK cells also express numerous iNKR. Even though inhibition of NK cell pathway had both upregulation (LILRB1, AIRM1, NKG2A) and down-regulation (LAIR1), the downstream gene had minor changes, indicating minor changes of NK cell inhibition in the SIV-infected long-term nonprogressing status.